To find out how lung surface active material (SAM) absorbs so rapidly to the air water interface, and spreads as a monolayer; then how some components separate, and are squeezed out of the monolayer on compression; and then how the dipalmitoyl phosphatidylcholine-rich (DPPC) monolayer collapses. Methodology 1) Determine the speed and extent of adsorption of SAM components at the air/water interface. We will use Teflon dishes with 30 ml of buffer and measure surface pressure (Pi) with a strain guage, surface potential (Delta V) with an ionizing electrode and surface accumulation of betaradioactivity with a Geiger or gas flow counter. SAM fractions will be prepared by density gradient centrifugation, other lipids will be purified just before use. Adsorbed monolayer material will be collected and prepared as surface replicas and thin sections for electron microscopy. 2) Determine the speed and extent of SAM lipid and protein segregation, squeezeout (of spreading agents), and collapse (of DPPC). A Langmuir/Wilhelmy surface balance will be used at 37 degress C in the servo mode, measuring Pi, Delta V and surface radioactivity with sampling for morphology. We will use the same SAM and lipids as in 1). Long Term Objectives 1) understand how SAM works and is handled by the body. 2) Develop criteria for an atrificial SAM to be used in treating Respiratory Distress Syndrome of the newborn.